14 September 1968

Papers and Originals

Control of Pain in the Rheumatic Disorders*

F. DUDLEY HART~t M.D., F.R.C.P.

But. med. Y., 1968, 3, 635-640

Summary: Pain may be attacked in the rheumaticdiseases (1) centrally, with drugs ranging in efficiency

from those which are potentially addictive and under theDangerous Drugs Act (e.g., pethidine) and are thereforerarely used, down to simple analgesics such as paracet-amol; (2) peripherally, by local action, whether it be byapplications of heat or cold, by injections of local anaes-

thetics or anti-inflammatory agents, or by surgery; (3)peripherally, by anti-inflammatory non-analgesic agentstaken systemically, such as the corticosteroids; and (4)peripherally, by anti-inflammatory-analgesic-antipyreticagents taken systemically, such as aspirin.The exact sites of action of the pyrazoles, indomethacin,

the anthranilic compounds, and other anti-inflammatory-analgesic-antipyretic drugs are as yet uncertain, but alongwith these methods of attacking the pain-producing areas

help must also be given to the distressed mind behind thejoints. Faith in the future, cheerfulness, freedom fromdepression, and the development of a philosophy to dealwith the uncertainties of the disease are essential. It hasbeen said that you don't have to be a doctor to treat un-

complicated lobar pneumonia: anybody with a bottle ofpenicillin in his hands holds the cure. It is the incurablediseases that are really worth treating, and that makedemands on the physician. To quote Tuker: "My lastword is this. Whoever has the care of a sorely strickenarthritic must encourage him to fulfil himself intellectuallyand spiritually, and to achieve-no matter what, but toachieve, so that he may nightly lay himself down on hisbed of pain looking forward happily to the morrow's task,mind centred upon it, no matter what it is; sticking instamps, research into anything you like, dabbling withpastel or water colours, writing chatty letters to friends.Anything at all, but let it be for him the most pressingthing of the day, and let him believe that you think it is.Help him and let him live, live fully."

This is perhaps the best analgesic of all.

Introduction

One who makes a study of the rheumatic diseases must makealso a study of pain, for the essence of and the central themethroughout these disorders is pain, and few people suffer asmuch continuous or intermittent day-to-day pain as thearthritic sufferer. A great deal has been written about thevirtues of pain. The late Reverend Dick Sheppard is reportedto have said to Laurence Housman: " I like pain: it bringsme nearer to my Master." But later, after more severe andmore continuous pain, he wrote: " I do not love suffering, so

*Based on a lecture given before the Willesden General Hospital Medi-cal Society on 15 May 1968.

t Westminster Hospital, London S.W.1.

you must not worry about me in that way. I dislike all thattalk about how lovely it is to suffer...A most gallant sufferer and one of the bravest men I have

ever known wrote a long and moving thesis on what it is liketo have rheumatoid arthritis: " I have the disease all over me:not one particle of me is untouched by it. As I sit here writingthis piece I have a sharp pain in my right shoulder, in my

right ear, in my right neck, in my right big toe, a bit of jabbingin my left neck and left jaw, and an ache in the scalp. If Iwere to move, I could at will set the rest of the orchestra onthe go: it is just tuning up" (Tuker, 1958).

After over 20 years of working with this group of patientsI am at the same time amazed and humbled when I see howmany more saints than sinners emerge from their suffering, andI marvel at the fortitude with which these patients endure theirdaily unpleasant ration of pain. This is a point that onlyrarely emerges from a clinical trial or a report on the efficiencyof some new form of treatment. Only the patient knows whathe experiences. It is a pity we cannot measure it in units:one dolour, perhaps, for the amount of discomfort one can takefor 10 minutes without reaching out for the next dose ofaspirin. It is interesting to compare these sufferers, whosepains are due to no fault of their own, with the luetic patientswith grossly deformed, ghastly looking Charcot joints whosuffer little or no pain, as the nerves are destroyed as partof the disease process. They walk cheerfully into their old agewith no discomfort whatsoever. If there is a moral here (whichI doubt), it is that most of the crippling and dysfunction is

not due to structural change, but simply and solely to pain.If I could give to the world one lastihg present before I die,it would be a superb non-toxic analgesic which took pain andstiffness away and allowed normal function-a sort ofheavenly aspirin or celestial codeine.No group of sufferers have so much continuous day-to-day

pain over such long periods as patients with chronic rheumaticcomplaints. This pain has to be controlled, for unrelievedpain breeds disuse and dysfunction, contractions and crippling,and few patients are so stoical as to need no analgesics on anyoccasion. The luetic sufferer with a grossly deranged anddeformed Charcot joint can still get about and lead an active,though restricted life, for he has no pain. Pain in an acutejoint lesion may perform a useful function by making thesufferer rest the affected member, but in a more chronic lesionit is more often essentially an evil thing, restricting function,inducing muscle wasting and crippling, and carrying with itmany psychological overtones.

Pain in the rheumatic diseases is a mixture of worry aboutthe future, annoyance at being unable to lead a normal life,nausea and dyspepsia on occasion from the medicamentsswallowed, rage at being told what to do by well-meaningfriends, stiffness, weakness, and local and general pain, andwith all this, not infrequently, a mental depression which maysometimes be severe and dominate the scene. Patients with aninflammatory arthropathy, such as rheumatoid arthritis, alsofrequently feel systemically ill, lose weight, and have fever and

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anorexia. For this extremely complicated, varied, and complexmixture of unpleasantness the word "pain" is mostinadequate. And just as in the laboratory experimentallyinduced pain becomes agony as time passes without relief, sothe very persistence of pain, its chronicity, multiplies andincreases the discomfort and psychic overtones.

Nature of Pain

One might imagine that in this year of grace, 1968, we knowfar more about the basic nature of pain than did our fathers.Such hardly seems to be the case, though we are probablymore conscious of our ignorance. As Graham Weddell (1966)said at the International Symposium on Pain at the HenryFord Hospital, Detroit, in October 1964, it seems improbablethat simple anatomical studies are going to be of much furtherhelp in the study of pain sensibility; they must be supplementedby histochemical and electrophysiological data before they canbe subjected to interpretation. Kruger (1966), at the sameconference, talking on the thalamic projection of pain, con-cluded that, although " pain " memories had been assumed toexist and that identifying the thalamic locus of such cells wouldclarify the basic problem of pain representation, an alternativeview would be that pain is not a sensory modality, but a com-plex response related to a certain variety of sensory events.Kruger says: " The quest for 'pain' neurons at moreperipheral levels has certainly been remarkably elusive. Is itpossible that neurons uniquely responsive to noxious stimuliare non-existent ?"Whatever the pathways, Beecher (1966) observed that many

years ago the point was made that in human suffering thereare two major components, the original sensation, or primaryphenomenon, and the psychological modification of it, thereaction or secondary phenomenon. The latter is a highlyindividual thing. The patient's mental reaction to the primarystimulus, his view of its seriousness and danger, may influencethe clinical picture greatly. Clinical pain can therefore notbe easily copied, and assessments of the effects of analgesicsmust in the final analysis be made on sufferers with diseaserather than normal subjects given artificial painful stimuli;as Beecher says, this is the difference between real and contrivedsensations.A patient was admitted to the wards under my care two

years ago in great distress. She had seen many specialists,and had had many investigations without a positive diagnosisbeing made. Over the previous 12 months her outstandingsymptom was of severe intractable pain in the lower thoraxwhich gave her no relief by day or night, and she was thenreceiving morphine or pethidine several times a day. Therewas such evident anxiety present that she was confidentlyreassured, and within a few days was needing only one or twodoses of dihydrocodeine in the 24 hours, and was sleeping wellwithout analgesics, merely removing her hearing-aid at night.Nevertheless, some months later a metastatic malignant lesionappeared at the site in question. The reaction to the painfulstimulus was clearly the important thing here, as it so often is.Fear and uncertainty are not only magnifying, but distorting,glasses.

Severe injury in the heat of battle may be painless: in theblitz, a patient on admission to our hospital complained of nopain, though her leg was connected only by a flap of skin tothe body. Beecher reported that in wounded soldiers in the lastwar about 25% needed medication to ease pain; 75% did not.In the civilian patients who had undergone usually less severemajor surgery these figures were reversed. In the one groupmany distractions were present; in the other the patient wasin a position where he anticipated and expected pain. I canmyself personally vouch for the great relief and ease of dis-omfort that comes to one as the ambulance enters the hospital

pard after one or two hours of uncertainty at the roadside.

Pain in Rheumatic Disorders-Hart JB AMEDICALJouPNAL

As a sense of security and relief flows in, anxiety and painsdiminish markedly. All who have worked with placebos knowhow effective they can be, and how clinical trials of analgesicsubstances must be devoid of emotional content of any sort.Though the patient must be aware of, and agree to, take part intheir trial, the exact time at which they are given should beunknown, not only to him, but to all taking part, otherwise thisplacebo effect, or its opposite-a nocebo response-may wreckresults.

Painful Stimulus

Let us start at the trigger, the point of pain. The skincovering the whole body is sensitive to pain. According toKellgren (1964) there are pain spots coinciding with specialnerve endings which form a rich subepidermal plexus andramify through all layers of the skin, a few penetrating as deepas the stratum granulosum, and this subepithelial plexussprings from the fine fibres of the peripheral nerves of thedeeper structures. The subcutaneous deep fascia, peri-osteum, joint capsules, ligaments, and sheaths of nerves andblood vessels are highly sensitive, but muscle, synovia, and fatare less so, while articular cartilage and compact bone areapparently insensitive to pain, giving rise to a sensation ofpressure only when artificially stimulated. From skin, muscle,and joints, the nerve impulse is carried through the peri-pheral nerves to the cord, leaving their cell station in theposterior root ganglia, entering the cord through the posteriorroots, and ending by synapse in the substantia gelatinosa ofthe posterior horns (Kellgren, 1964). Pain nerves from bloodvessels may follow a periarterial course at the periphery for somedistance before joining the nerve trunks. Pain arising in theskin is well localized, but pain of deeper structures may bediffuse and poorly localized.Those who have injected a tennis elbow or an acutely painful

rheumatoid elbow will often be surprised that not only thepain at the affected spot is eased, but also pain up and downthe arm from shoulder to wrist. Such local anaesthesia will-temporarily at least-abolish pain, but if a local tender spotis referred from a site elsewhere, although tenderness isremoved, pain and restriction of movement persist. Few painsin rheumatology are based on a simple peripheral pain spot,and even a so-called " tennis elbow," due usually to a forcefulbackhand shot causing injury to attachments of the commontendon of origin of the forearm extensors, may be productiveof secondary overtones. Nevertheless, local therapy may helpin easing pain: injections of hydrocortisone or a suitableanalogue or a local anaesthetic agent, local heat, or counter-irritation. The agonizing pain of a swollen, distended bursais rapidly relieved by incision and evacuation of some of itscontents; the same intense pain of tissues under tension alsooccurs in gout, an early whitlow, or a " hot Heberden's node"in its early acute inflammatory red state. Though this nodeis a manifestation of osteoarthrosis, essentially a degenerativecondition, it may start as an acutely painful condition in theterminal interphalangeal joint, which the patient may attackherself with a needle in an effort to ease the tension and relievethe pain. In the average rheumatic sufferer, however, whetherosteoarthritic, rheumatoid, or spondylitic, pain points aremultiple and most lie deeper, and local attacks on pain peri-pherally constitutes only a small part of the therapeuticprogramme.

Pain Threshold

It is of interest that although much attention has been paidto placebo reactors in clinical assessment of drugs given torelieve pain and great efforts have been made to pick twogroups of patients with similar extent and acuity of disease toreceive drug and placebo, little had been done to assess thepain threshold in such patients. We have attending the unitsome patients who are singularly uncomplaining, and who

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Pain in Rheumatic Disorders-Harthave very high thresholds to artificial painful stimuli. Thetwo most outstanding ones are both deeply religious, and havea complete faith in the Almighty and His medical servant, thephysician in charge of their case. One with severe unremittingrheumatoid arthritis of seven years' duration hobbled into theclinic, having never missed a day's work at her telephoneexchange. She made no complaint of pain, only difficulty ingetting about. Three years later she was wheeled into theclinic, still making no complaint of pain, and was found tohave fractures of necks of both femora and of one arm. Shewas not a hysteric and was mentally normal, though not highlyintelligent, and her pain threshold was higher than that ofanybody then working in the clinic, as judged by Hollander'stest (Hollander, 1939).

Singularly little work has been done on this question of painthreshold in the rheumatic diseases, though for many years wehave used Libman's sign in the clinic (Libman, 1934). This isa rough measure of individual pain threshold: firm pressure inthe normal subject to the mastoid being painless, to the styloidprocess painful. Though a very crude method, it is occasion-ally useful in separating the normal average from the hypo-sensitive subject.

In 1954 Keele reported the use of a pressure algometer,applied to the forehead, which correlated closely with othermethods such as the forearm ischaemic method of Lewis (1942),and the method of Hollander (1939), where pain is producedby tightening a blood-pressure cuff applied round a small nut-meg grater above the elbow. More recently Keele (1968),using the pressure algometer, was able to divide patients withcoronary thromboses into high, normal, and low thresholdcategories: severity, extent, and duration of pain and morphinerequirements were all found to be diminished with raising ofthe pain threshold. We have used Hollander's method in thepast, and are now carrying out a study with Keele's algometer.It has for some time seemed clear to us that relapses withincrease of pain in rheumatoid arthritis may be true, due toincreased activity of the disease, or false, due to altered moodarising from depression or other factors of psychogenic nature.Studies of pain threshold might well prove informative here.

Morning Stiffness

Immobility in bed at night is characteristically and typicallyfollowed by increased swelling, tenderness, pain, and stiffness inthe joints in the morning in active rheumatoid disease. Theearly morning is usually the worst time in the 24 hours for therheumatoid sufferer. Morning stiffness and pain may also bemarked in lumbar disc disease, and pain is common in cervicaldisc disorders, the early morning after rising being the mostpainful period in the 24 hours. In giant-cell arteritis morningstiffness and pain in shoulder and hip girdles may be verypronounced. In patients with ankylosing spondylitis the morn-ings are also usually the worst time for pain and stiffness, thetissues in both diseases "gelling" in the night.

Swelling of fingers has been shown to be more pronouncedin the mornings in rheumatoid arthritis (Boardman and Hart,1967), and many spondylitics voluntarily rise in the night once

or several times to prevent the morning stiffness, which maylast anything from an hour to half the day. To prevent it,corticosteroids may be given by mouth on retiring, or indo-methacin by mouth or by suppository. We have found theindomethacin 100-mg. suppository to be more efficient in thisrespect than the 250-mg. suppositories of phenylbutazone or

oxyphenbutazone. Holt and Hawkins (1965) found that indo-methacin suppositories give satisfactory blood levels, and theremay be less likelihood of dyspepsia with their use, though, as

with phenylbutazone suppositories, it may still occur. Theduration of therapeutic action of aspirin and most of its sub-stitutes taken on retiring is too short to have much effect inthe early morning, though phenylbutazone and oxyphen-

BRMnI UMEDICAL JOURNAL 637

butazone, because of their prolonged action, may, taken orallyday by day, exert a beneficial action through the night.

SpasmSpasm is a word often used in medicine, and even more

often abused, for nothing is easier than to explain transientsymptoms by postulating a temporary contraction of skeletalor arterial muscle. Much of this so-called spasm is a suddenvoluntary muscular contraction to anticipate or prevent pain, orit may be a true hyperreactive stretch reflex. True muscle spasm,nevertheless, may accompany severe deep pain of more thantemporary duration (Lewis and Kellgren, 1939). For instance,6% saline injected into muscles of the trunk produces seg-mental pain and rigidity of the appropriate segment, possiblyas a result of a spinal reflex. In the limb segmental muscula-ture is more widely distributed, with the result that musclespasm appears as widespread fine fasciculation, demonstrableby electromyography, though less readily clinically. It hasbeen suggested (Simons et al., 1943) that this reflex motoractivity may lead to local muscle fatigue and to secondarypain arising in the muscles themselves, and this theory wasoften used in wards and clinics to explain pains arising aroundpainful joints and apparently in the muscles serving thesejoints. The bulk of evidence, however, is in favour of thepainful joint being the culprit, for if effectively relieved bylocal therapy pain in the surrounding muscles is also relievedat the same time, the so-called " spasm-pain" being referredfrom the affected joint. I have on two occasions seen localizedspasm and rigidity of one rectus muscle, that is, unilateralboarding of the abdomen; in one case it was due to infection,and in the other to haemorrhage, muscle rigidity rapidlyresolving on evacuation of blood or pus from the rectus sheath.

Drugs

The drugs available for the relief of pain in the rheumaticdisorders fall into the following categories:

(1) Simple analgesics without demonstrable anti-inflammatoryaction (for example, paracetamol; codeine; dihydrocodeine;dextropropoxyphene.

(2) Analgesics with anti-inflammatory and antipyretic action (forexample, acetylsalicylic acid; the pyrazoles, phenylbutazone andoxyphenbutazone; the anthranilic compounds, mefenamic andflufenamic acids; indomethacin).

(3) Analgesics potentially addictive and therefore rarely used(for example, dipipanone; pethidine; morphine). Pentazocine isunusual in being apparently not addictive.

(4) Anti-inflammatory agents without analgesic properties (forexample, the corticosteroids and corticotrophin).

(5) Psychotropic agents which, by altering mood, help to easepain: antidepressants (for example, imipramine; amitriptylinee;protriptyline; monoamine oxidase inhibitors (for example,iproniazid, isocarboxazid, tranylcypromine; phenelzine, etc.) ;

tranquillizers and sedatives (for example, chlordiazepoide ;

barbiturates; meprobamate; diazepam); stimulants (for ex&ampl%amphetamine; methyl and dexamphetamine, usually given wdihamylobarbitone).

(6) Long-term anti-inflammatory agents, the action of which isnot understood (for example, guld salts; chloroquine).

(7) Agents possibly acting on lysosomes (for example, colchicine).(8) Immunosuppressive agents (for example, chlorambucil;

azathioprine, still in the experimental phase as regards treatment ofthe rheumatic disorders, and potentially dangerous).

(9) Agents which, by improving general health, may raise thepain threshold (for example, iron; blood transfusions; vitamins).

It is clear that with such a large part of the British Pharma-copocia available and potentially helpful the prescriber's partis not a simple one. The basis of therapy lies essentially andusually in groups 1 and 2; group 4, the corticosteroids, areextremely useful, but must be used in conservative dosage (7

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mg. of prednisone or less daily for continual therapy), for thebad reputation they have earned in the last 18 years has beenlargely due to prolonged overdosage. Preparations containingtwo or more drugs, very popular in the past, still continue tobe popular; in a recent MIMS 67 out of 101 analgesics listedwere of this nature. Only rarely do such mixtures have anygreat advantage over single substances. Most aspirin com-pounds still contain phenacetin, for instance, which, on presentevidence, is both toxic and unnecessary. If more than onedrug is necessary for the rheumatic sufferer, as it often is, inmost cases they are best prescribed individually in the minimaleffective dosage. Drug therapy in the rheumatic disordersshould be like climbing a ladder: one starts at the bottom andgoes up only as far as is absolutely necessary.

Rheumatoid Arthritis

Rheumatoid arthritis is the disorder par excellence where allsecondary pain factors come into play. Many affected areasdischarge repeated pain stimuli from several joints, and, inaddition, systemic illness and psychological overtones add toand complicate the picture. The treatment of this difficult andprolonged disorder makes more demands on the physician thanalmost any other condition. Not only must appropriate anal-gesics be supplied, but also trust, some affection, sympathy, andunderstanding, all of which help to relieve the patient's " pain."Drugs on the D.D.A. list should rarely, if ever, be used, forthe risks of addiction in such cases are very real; but, of theothers, the popular ones are acetylsalicylic acid in some form,paracetamol, codeine or dihydrocodeine bitartrate, aspirin-phenacetin tablets (phenacetin is very rarely prescribed alone),dihydrocodeine, phenylbutazone, and oxyphenbutazone, and,more recently, dextropropoxyphene, mefenamic and flufenamicacids, and indomethacin.The choice from these depends on effect and tolerance in the

individual case, but usually aspirin in some form is used first,usually four- to six-hourly in doses of 0.6-1 g. (10-15 gr.).Boardman and I (Boardman and Hart, 1967) have shown thatdaily doses up to 2-3 g. have an analgesic action, but thatlarger doses are necessary to produce blood and tissue levelswhich have a measurable anti-inflammatory effect on the fingersof rheumatoid sufferers. Only if aspirin fails or produces toxiceffects are other substances tried. Whatever programme of rest,exercise, and physiotherapy is used, whether gold salts, anti-malarials, or surgery, the vast majority of patients will needanalgesics occasionally or, usually, regularly. From interviewswith five patients, each of whom had had rheumatoid arthritisfor more than 30 years uninterruptedly, of all of the manytherapeutic agents used over these years aspirin was placedfirst, usually in soluble form. This was the agent which hadover the years given them most relief with least side-effects.Though salicylates usually cause slight blood loss in the stoolsif given repeatedly, this is not usually accompanied bydyspepsia, and only occasionally are they productive of severeanaemia.

Phenacetin is much less popular now than it was, and in ouropinion should be deleted from compound analgesic tablets, asReckitts have recently done with their soluble effervescent com-pound codeine tablets (Codis). We removed it at WestminsterHospital, and increased the aspirin and codeine, in 1955 andthis modified tab. codein. co. remains very popular with thepatients. The case against phenacetin as an agent toxic to thekidney may be incomplete, as phenacetin is never given alonebut always in combination with other drugs, but in all prob-ability it is the agent responsible for necrosis of the renal papillaand damage to the renal parenchyma. Apart from this toxiceffect, sulphaemoglobinaemia and methaemoglobinaemia arealso real and well-proved complications.

Exacerbation of rheumatoid arthritis may be triggered off bya number of factors: changes in or stopping treatment, infec-

Pain in Rheumatic Disorders-Hart B ORNAMEDICAL IOURNAL

tion, overexertion, or trauma. Such acute episodes may bepolyarthritic or confined to one or two joints; if the latter,trauma or local infection may be responsible, and any ugly,swollen, hot joint should be aspirated lest it be due to apyarthrosis, for rheumatoid joints are easily infected andpyaemia, particularly with the Staphylococcus areus, is notuncommon. General exacerbation of the disease is best treatedby bed rest, higher dosage of analgesics, and perhaps by a shortcourse of injections of corticotrophin, preferably as an inpatient.This may bring the disease under control more rapidly thanmost agents, and dosage may be gradually reduced and dis-continued after 10 to 20 days; though rebound may occur, theprevious therapy may subsequently often be adequate tocontrol the disease.

Corticosteroids may be used, but conservative dosage under7 mg. of prednisone or its equivalent is unlikely to be sufficient,and high dosage will produce adrenal suppression and in timeother unwanted effects if dosage cannot soon be reduced. Foracute pain the addition of tinct. opii 71-20 iims (o.5-1.3ml.) to 10-20 g. (0.65 to 1.3 g.) of aspirin in a freshly mademixture is very useful, but aspirin in this form soon deterioratesand may quickly become a powerful gastric irritant. A similarparacetamol-cum-opio mixture containing 1.5-2 g. of para-cetamol does not have this drawback. Substances under theD.D.A. are best avoided, though dipipanone or the compounddipipanone plus cyclizine hydrochloride (Diconal) may beuseful taken rarely and not repeatedly. Injections of dihydro-codeine bitartrate 50-100 mg. may be useful if there is. vomit-ing or nausea, and suppositories of indomethacin or phenyl-butazone or oxyphenbutazone may be helpful under thesecircumstances: the former in my experience are the moreeffective.

Osteoarthrosis

Pain may be caused by a number of different mechanisms inosteoarthrosis. The rapidly developing " hot Heberden " nodeis an inflammatory process, the red, inflamed area being tenseand distended. The condition subsides over a period, usuallyof several weeks, and is gradually replaced by the usualdegenerative changes in the terminal interphalangeal joints ofthe fingers. Pain arising from the distal interphalangeal jointsis notoriously difficult to treat, hot water or wax or cold com-presses usually having little effect, and sometimes aggravatingthe condition. Analgesics are only partly helpful, and sedativesand hypnotics such as barbiturates, or a combination of both,may prove as useful. Osteoarthrosis in neck, hip, knee, andlumbar spine all call for different approaches-rest, immobility,exercises, passive movements, traction-according to the siteand type of pain. Happily, most osteoarthrotic pains abate,even occasionally in hip and knee, though in these sites painsare usually persistent and unremitting.

Efforts to break pain cycles by neurectomy, sympathectomy,and nerve blocks have been usually unrewarding, and in manycases bone surgery offers the only hope of pain relief. Of theusual analgesics, indomethacin and the pyrazoles are oftenhelpful, as may be any of the other analgesic agents, but relief isusually only partial. Overuse and underuse in bad positionsmay aggravate osteoarthritic hips; for instance, walking orstanding overlong on hard pavements or sitting for prolongedperiods with legs in right-angled flexion. The one hip move-ment which is maintained fully without major discomfort isflexion; where all other movements are completely lost, thisremains because the patient performs this one hip movementrepeatedly throughout the day in sitting and standing. InIndian patients' hips the range of movement is usually greaterbecause of the more complete range of movement performedin the day.

Adequate analgesia may help maintain function by allowinggreater mobility and more effective exercises. As in rheumatoidarthritis, psychotropic drugs may be helpful in certain cases.

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Pain in Rheumatic Disorders-Hart

Pain of Arteritis

The severe, sheep-cell agglutination test positive, rheumatoidsufferer with advanced disease may start to complain of achesand pains of a new order in areas away from joints, in abdomenand thorax as well as in the extremities, unrelated in time andseverity to his many articular pains. Such pains may bethought occasionally to be due to ischaemic heart disease,appendicitis, pelvic infection, or a variety of other causes.Their origin is in the arteritic changes that are a part ofadvanced rheumatoid disease; they are difficult to treat, andcarry a bad prognosis. Other polyarteritic manifestations,such as gangrene of the extremities, are obvious from the start,but low-grade or acute thoracic or abdominal pains are less easyto diagnose. Neuropathic features carry their own particularblend of discomfort-a cocktail of numbness, discomfort, andodd sensations that are different from, and are added to, thebackground of articular pains.

The arteritis seen in older patients of giant-cell type gives acharacteristic severe temporal headache in classical cases oftemporal arteritis, but the marked stiffness, worse in the morn-ings, and pains in shoulder and pelvic girdle areas are oftenmisdiagnosed in those cases where temporal vessels are spared.The markedly raised sedimentation rate, often over 70 mm.

in one hour (Westergren), is a pointer to the correct diagnosis.Arteritic lesions in polyarteritis nodosa and disseminated lupuserythematosus may cause lesions in any system, and in theirearly stages respond, as do most inflammatory arteritic lesions,better to an effective anti-inflammatory drug such as thecorticosteroids than to anything else. It is not without interestthat anti-inflammatory drugs help greatly in most of therheumatic disorders, and most of the drugs which have anal-gesic properties have also an antiphlogistic action. The oldestof them, aspirin, has been shown to act peripherally, and notcentrally as we were taught as medical students (Lim, 1966).

Ankylosing SpondylitisIn this condition, as noted above, the morning stiffness which

makes life miserable for so many rheumatoid sufferers ispresent, usually in marked degree. It is immobility in anky-losing spondylitis that produces aggravation of stiffness andpain, and the basis of therapy is therefore a programme ofactive exercises and relief of pain by drugs, so that a moreactive life can be led with greater freedom of spinal and hipmovements. Aspirin is sufficient in mild cases, but, for many,indomethacin, oxyphenbutazone, or phenylbutazone is neces-sary, indomethacin also proving useful taken in suppositoryform at night to relieve morning stiffness. Orthodox therapybefore the war lay in immobilizing the patients in plaster castsand jackets. to achieve a good spinal position, overlooking thefact that function is more important than posture. Suchtherapy, by increasing stiffness in hip and spine, often pro-duced crippling, and the lucky spondylitics in those days werethose who were not correctly diagnosed, and were thereforenot "correctly " treated.

A dangerous misdiagnosis was that of tuberculosis of boneand joint, for the two conditions may resemble each otherquite closely in spine, hip, and other joints, the lytic lesionin spondylitis being mistaken for a tuberculous erosion.Immobility, useful in the one, is disaster in the other (Hart,1968). Immobility of chest wall similarly leads to reducedrespiratory function (Hart, Emerson, and Gregg, 1963), and anactive, energetic, preferably outdoor life is better for thesesufferers than one spent bent over desk or drawing-board,not only as regards spinal but also respiratory function: regularplaying of the bagpipes helped one of my patients. Breathingexercises, though admirable, areless effective than the over-

breathing of an energetic job. Effective pain relief, by increas-ing function, is therefore sound therapy, and phenylbutazoneand oxyphenbutazone by their even, prolonged action over the

ORNALMEDICALJOURNA

24 hours are very useful drugs. Indomethacin is also usefuland has less danger of causing a blood dyscrasia. Any of theother analgesics may also be effective mi different cases. Localdeep x-ray therapy to the spine, the treatment of choice justafter the war, has gone out of fashion because of the dangersof induction of leukaemia, but it does frequently relieve symp-toms effectively (Hart, 1961), though only occasionally forperiods of more than a year.

Gout

The agony of acute gout is usually a stage beyond that ofthe pain experienced in the other arthropathies. It matches thepain of a fracture recently enclosed in a too tight plaster. Itis caused by acute inflammation in tissues which cannot readilyexpand, and is one of the most severe pains which can beexperienced. A patient of mine who had an attack of goutfollowing an acute coronary occlusion told me that it was themore severe of the two. This is usually " straight " or primarypain. The sufferer knows what it is, knows he is not going todie of it, and has no particular fears of complications, but itis a severe, agonizing pain just the same. Rapidity of painrelief is therefore important, and in our unit we place indo-methacin first in efficiency (Boardman and Hart, 1965),phenylbutazone or oxyphenbutazone second, and colchicinethird. Phenylbutazone may be given effectively by intra-muscular injection (250 mg.), and colchicine may be givenintravenously with great effect, though it is not without danger,and should not be repeated within eight hours. Death hasoccurred under such circumstances. Corticosteroids or cortico-trophin are usually no more effective, but may be necessary inresistant cases. It is amazing how often sulphinpyrazone,probenecid, or allopurinol is mistakenly used in general prac-tice for the control of an acute attack; these drugs have, ofcourse, no effect on the acute, painful process, and are likelyto precipitate further acute episodes when started de novo.

Bursitis

The pain of acute bursitis is often misdiagnosed, for it isoften referred away from the primary site, or it may arise frombursae the existence of which the clinician has forgotten.Bywaters (1965) has referred to the large number of bursae-around 156-in the body. These can all become inflamedeither locally or as part of a generalized rheumatoid arthritis,where they add considerably to the signs and symptoms of thisdisorder. There are, for instance, small bursae between themetatarsal heads, beneath the insertions of the psoas, and,according to Monro (1788, 1799), 18 in the hand, 6 around theelbow, 8 around the knee, and 14 around the hip-a total, asstated above, of 78 on each side of the body. They may becomedistended with viscous paste-like material, and sometimes withpus, and incision and evacuation may give immediate relief.When they are part of a rheumatoid process, aspiration (ifpossible) and installation of a locally acting corticosteroid mayhelp, as in knee (semimembranosis) and shoulder (subacromial).Rheumatoid disease affects also tendons and synovial sheaths,and these form very characteristic and diagnostic swellings,one of the commonest being the involvement of the extensorsheaths on the backs of the hands. These are, however, rarelypainful. It is the lesser-known and deeper bursae which maycause diagnostic difficulty. Injection of a local anaestheticinto the painful area may give relief if accurately sited.

Compression (Entrapment) NeuropathyUntil a few years ago the typical painful paraesthesiae of

median nerve carpal-tunnel compression was attributed to anumber of causes. Now, even if part of some other diseaseprocess such as amyloidosis with multiple myelomatosis, or

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640 14 September 1968 Pain in Rheumatic Disorders-Hartrheumatoid arthritis, surgical division of the transverse carpalligament usually gives rapid and complete relief. Other com-pression neuropathies may occur, as of the ulnar nerve by thearcuate ligament below the elbow (Osborne, 1957), in the feet,and elsewhere. The subject is discussed in some detail byThompson and Kopell (1959) and by Kopell, Thompson, andPostel (1962). Treatment lies in the localization of the com-pression and surgical release of the compressed nerve.

REFERENCESBeecher, H. K. (1966). In Pain, edited by R. S. Knighton and P. R.

Dumke, p. 221. London.Boardman, P. L., and Hart, F. D. (1965). Practitioner, 194, 560.Boardman, P. L., and Hart, F. D. (1967). Bnt. med. Y., 4, 264.Bywaters, E. G. L. (1965). Ann. rheum. Dis., 24, 215.Hart, F. D. (1961). Clin. Radiol., 12, 130.Hart, F. D. (1968). Lancet, 1, 740.Hart, F. D., Emerson, P. A., and Gregg, I. (1963). Ann. rheum. Dis.,

22, 11.Holander, E. (1939). 7. Lab. clin. Med., 24, 537.

Holt, L. P. J., and Hawkins, C. F. (1965). Brit. med. 7., 1, 1354.Keele, K. D. (1954). Lancet, 1, 636.Keele, K. D. (1968). Brit. med. 7., 1, 670.Kellgren, J. H. (1964). In Textbook of the Rheumatic Diseases, 3rd ed.,

p. 14, edited ba W. S. C. Copeman. Edinburgh and London.Kopell, H. P., Thompson, W. A. L., and Postel, A. H. (1962). New

Engl. 7. Med., 266, 16.Kruger, L. (1966). In Pain, edited by R. S. Knighton and P. R. Dumke,

p. 67. London.Lewis, T. (1942). Pain, p. 97. New York.Lewis, T., and Kellgren, J. H. (1939). Clin. Sci., 4, 47.Libman, E. (1934). 7. Amer. med. Ass., 102, 335.Lim, R. K. S. (1966). In Pain, edited by R. S. Knighton and P. R.

Dumke, p. 117. London.Monro, A., secundus (1788). A Description of all the Bursae Mucosae

of the Human Body.. Edinburgh.Monro, A., secundus (1799). Abbildungen und Beschreibungen der

Schleimsiicke des Menschlichen Korpers, edited by J. C. Rosen-miller. Leipzig.

Osborne, G. V. (1957). 7. Bone 7t Surg., 39B, 782.Simons, D. J., May, E., Goodell, H., and Wolff, H. G. (1943). Ass. Res.

nerv. Dis. Proc., 23, 228.Thompson, W. A. L., and Kopell, H. P. (1959). New Engl. 7. Med.,

260, 1261Tuker, Sir Francis (1958). Personal communication.Weddell, G. (1966). In Pain, edited by R. S. Knighton and P. R. Dumke,

p 3. London.

Use of Capillary Blood in Measurement of Arterial Po.

J. MAcINTYRE,* M.B., CH.B.; J. N. NORMANI M.D., PH.D., F.R.C.S.; GEORGE SMITH4t M.D., CH.M., D.SC., F.R.C.S.

Brli. mad.Y., 1968,3, 640-643

Sumary: In this study we investigated the possibilityof obtaining accurate values of arterial Po. from

specimens of capillary blood stored in glass capillary tubesand measured in an oxygen microelectrode. It has beenshown that Po2 measurements made on the Radiometeroxygen microelectrode are as accurate as those made onthe macroelectrode and that the storage of blood is assatisfactory in glass capillary tubes as in glass syringes.The important feature in obtaining accurate values forarterial Po1 is the choice of the capillary bed and itsmethod of preparation for sampling. If the ear lobe ismassaged with thurfyl nicotinate (Trafuril) it is possibleto obtain values of PoN from the capillary blood which arein close agreement with arterial Po2 in normal, hyperoxic,and shocked vasoconstricted patients.

Introduction

There is an increased awareness of the need to monitor theblood oxygen tension when efficient systems of oxygen admini-stration are used in the management of severely ill patientssuffering from a variety of anoxic conditions. It is of con-siderable importance to maintain adequate tissue oxygenationin states of stagnant anoxia until the underlying pathology iscorrected, and where hyperbaric oxygen techniques are usedfrequent arterial Po. measurement is needed if oxygen poison-ing is to be avoided (Norman and Smith, 1967). Capillaryblood specimens can now be used for a variety of biochemicalmeasurements, and with the recent advent of the oxygen micro-electrode it should be possible to use specimens of capillaryblood as an index of arterial oxygen tension. This wouldfacilitate the management of patients receiving oxygen atnormal and increased atmospheric pressures and may proveinvaluable in paediatric practice, where repeated arterialsamples are less easily obtained. Initial attempts to correlate

capillary blood Po2 and arterial Po2 proved unsatisfactory,however, and this study was devised to assess the errorsinherent in making such measurements.Various electrode systems have been used to measure blood

oxygen tension (Staub, 1961; Elridge and Fretwell, 1965;Johnstone, 1966; Moran, Kettel, and Cugell, 1966; Rhodesand Moser, 1966). Considerable errors can, however, be madeif care is not taken in calibration of the electrode (Moran et al.,1966; Rhodes and Moser, 1966; Adams and Morgan-Hughes,1967), in the sampling of blood (Nunn, 1962; Johnstone,1966), and if allowance is not made for time lapse betweensampling and measurement (Nunn, 1962 ; Elridge and Fretwell,1965 ; Lenfant and Aucutt, 1965; Johnstone, 1966). In prac-tice the latter may be the most important source of error ifthe measurements are made in a laboratory situated at somedistance from the patient.

It seemed desirable to evaluate (1) the accuracy of the oxygenmicroelectrode in the measurement of Po2 of blood containedwithin glass capillary tubes as compared with that of the macro-electrode in the measurement of blood contained within glasssyringes; (2) the rate of decline of Po2 of blood stored inglass capillary tubes, glass syringes, and plastic syringes, andto observe the effect of time, temperature, and initial oxygentension on these three storage methods ; and (3) the importanceof the capillary sampling site and the mode of preparation ofthe capillary bed previous to sampling i different states ofperipheral perfusion.

* Research Fellow in Surgery, University of Aberdeen.. Lecturer in Surgical Science, University of Aberdeen.Regius Professor of Surgery, University of Aberdeen.

Methods

The oxygen electrodes used were the Radiometer micro-electrode (Radiometer Ref. E5046) and the Radiometer macro-electrode (Radiometer Ref. E5021). The electrodes were cali-brated with nitrogen, air, and oxygen which had been warmedand humidified by passage through sintered glass humidifiersimmersed in a thermostated water-bath maintained thermo-statically at 37° C. The use of gases allowed the calibration

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